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Pharm CLS > Kessel1 > Flashcards

Kessel1 Flashcards

1
Q

Properties of malignant cells

A

evade apoptosis, self sufficiency in growth signals, insensitivity to anti growth signals, tissue invasion and metastasis, limitless replicative potential, sustained angiogenesis

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2
Q

Why use chemotherapy?

A

precise sites of neoplasia can be difficult to detect. need to seek out and eradicate.

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3
Q

What are the major classes of drugs for cancer?

A

antimetabolites (inhibit DNA syn)
Alkylating agents (impair DNA fxn)
Antibiotics (DNA binders)
Hormone antagonists (inhib receptor fxn)

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4
Q

How does methotrexate function?

A

Blocks the transfer of 1 carbon fragment from Uracil to thymine. DNA synthesis STOPS.. Inhibits the enzyme dihydrofoilic reductase

antagonizes the synthesis of thymidyic acid, precursor of dna

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5
Q

Resistance of 5FU looks at what?

A

impaired transport system! selection for tumor cell with high DHFR levels

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6
Q

What is an example of an S-phase specific drug? how does it function?

A 
Cytosine arabinoside (Ara-C)
incorporated into DNA,terminates DNA chain elongation,inhibits DNA polymerase
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7
Q

Gemcitabine specs

A

Targets G0/G1 cells–accum of S phase cells.

Incorporated into DNA + inhibits ribonucleotide reductase

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8
Q

Alkylating agents preferentially attack?

A

DNA guanines- cross link impair strand separation and DNA/RNA synthesis is impaired. Response increase by lack of repair enzymes

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9
Q

How can we circumvent MTX toxicity?

A

supply a cell with folinic acid, a reduced folate

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10
Q

5-FU is enzymatically modified to its functional form…?

A

FUdRP- potent inhibitor of thymidylate synthesis

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11
Q

What are the components of the triple complex that inhibits enzyme function?

A

FUdRP, reduced folate, enzyme thymidylate synthetase

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12
Q

FU is inactivated by WHAT

A

the enzyme DPD! dihydropyridinede hydrogenase

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13
Q

In general, how do the alkylating agents function?

A

Agents transformed into highly reactive structures toward all nucelophilic groups. Alkylated DNA cannot function properly during replication, synthesis inhibited. Treatslowly-dividing cancer cellsunresponisble to antimetabolites.

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14
Q

What is nitrogenmustard (HN2)

A

A very powerful alkylating everything.Alykates sites onseparate strandsofDNA,cross-linking DNA strands. cannot replicate! TWoothers: mlphalan, chlorambucil!takenorally and broader spectrum.

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15
Q

Benefits of Cyclophosphamide

A

Broad spectrum,given orally (require activation by liver enzymes)

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16
Q

MESNA

A

drug that can neutralize the inflammatory drug metabolites of CTX that concentrate in the bladder

17
Q

How does temolozolomide work???

A

Once activated, the product can be mistaken for adenine! so, base-pair mismatching! eventual los of viability

18
Q

Cis Platinom MOA

A

after loss of thechlorineatoms, drug acts similar to alkylating agent, covalent bondwithaminoresidues ofucleic acids. littlecell-cycle specificity.

DNA crosslinker, renalexcretion, can cause hearing loss, limitingtox: renal! distortion of the DNA strandcaused by binding of amolcule of cisPT notrecognizined by DNA repair enzymes in malignant cell lines. permaenent damage and todna replication andcelldeath.

19
Q

Drug resistance patterns

A
  1. decreased entry into orincreased loss from cell.
  2. drug inactivated within cell
  3. enhanced DNA repair after alkylation
20
Q

Actinomycin D

A

antibiotic that bindstightly toDNA,inhibitingRNAsynthesis.No covalent bonds withDNA but fitsINTOa portionofthehelicalstrucutre(INTERCALATION)

21
Q

Bleomycin

A

Results in breakin gand fragmentation of theDNA strands! drug concentratesinskinand lung, no marrow toxicity.

22
Q

Doxorubicin

A

binds to DNA,inhibits subsequent synthesis. can also bind tonondefinng andpromote cell death inhibit cellviability via interactions with topoisomerase II.

23
Q

ANthracycins!

A

bnefit! doxorubicin! broad spectrum efiacy. tox BM and heart muscle. Cardic muscle toxicity!! FREE RADICALS!!

24
Q

VINCA alkaloids!

A

arrest cell division at metaphase by disrupting microtubule structures. Also neural MT- neurotox.

25
Q

Taxol

A

promotes tubulin polymerization and stability of MT… (vincas promotemicrotubule dissociation) Inhibit metaphase and mitosis! Chemotherapy additive disables side effect.

26
Q

Camptothecin

A

Topoisomerase I antagonist

27
Q

Etoposide

A

Topoisomerase II inhibitor. tox to GI tract and bone marrow

28
Q

Multidrug resistance

A

transport system that pumps drugs out of cells! protective to normal cell types. missing in malignant cells.

29
Q

Gleevec (imitinib)

A

SO HELPFUL for CML!! interrupts the phosphyrlation of several substrates that activate growth signals

30
Q

Monoclonals

A

Erbitux-targets egrf
avastin- targets vegf
Herceptin targets her2neu

31
Q

Cytotoxic action of MTX antagonized by ?

A

combination of thymidine and folinic acid!

32
Q

How can MTX possibly antagonize 5FU?

A

ohhhhhh you know, MTX limits folinic acid production. necessary for 5FU’s triple complex

33
Q

5FU resistance is caused by WHAT?

A

TUMOR CELL DELETES ONE OR MORE ENZYMES INVOLVED IN THE PHOSPORYLATION OF FU

Pharm CLS (8 decks)

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